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Procell Inc tnbc cell lines mda mb 231
CEP exerts cytotoxicity in TNBC cells. (A) Chemical structure of CEP. (B) CEP inhibited TNBC cell viability. The effect of CEP treatment on TNBC cell viability after 24, 48 and 72 h. (C) CEP inhibited <t>clonogenicity</t> <t>of</t> <t>MDA-MB-231</t> and Hs578T cells. n=3; *P < 0.05, **P < 0.01 and ***P < 0.001 vs. control. CEP, cepharanthine; TNBC, triple-negative breast cancer.

CEP exerts cytotoxicity in TNBC cells. (A) Chemical structure of CEP. (B) CEP inhibited TNBC cell viability. The effect of CEP treatment on TNBC cell viability after 24, 48 and 72 h. (C) CEP inhibited <t>clonogenicity</t> <t>of</t> <t>MDA-MB-231</t> and Hs578T cells. n=3; *P < 0.05, **P < 0.01 and ***P < 0.001 vs. control. CEP, cepharanthine; TNBC, triple-negative breast cancer.

Tnbc Cell Lines Mda Mb 231, supplied by Procell Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Cepharanthine inhibits lysosomes and induces apoptosis in triple-negative breast cancer cells"

Article Title: Cepharanthine inhibits lysosomes and induces apoptosis in triple-negative breast cancer cells

Journal: Molecular Medicine Reports

doi: 10.3892/mmr.2026.13899

Figure Legend Snippet: CEP exerts cytotoxicity in TNBC cells. (A) Chemical structure of CEP. (B) CEP inhibited TNBC cell viability. The effect of CEP treatment on TNBC cell viability after 24, 48 and 72 h. (C) CEP inhibited clonogenicity of MDA-MB-231 and Hs578T cells. n=3; *P < 0.05, **P < 0.01 and ***P < 0.001 vs. control. CEP, cepharanthine; TNBC, triple-negative breast cancer.

Techniques Used: Control

CEP induces apoptosis in triple-negative breast cancer cells. Flow cytometric quantification of apoptosis induced by CEP in (A) MDA-MB-231 and (B) Hs578T cells (n=3; 48 h). **P<0.01 and ***P < 0.001 vs. control. CEP, cepharanthine; ns, not significant.

Figure Legend Snippet: CEP induces apoptosis in triple-negative breast cancer cells. Flow cytometric quantification of apoptosis induced by CEP in (A) MDA-MB-231 and (B) Hs578T cells (n=3; 48 h). **P<0.01 and ***P < 0.001 vs. control. CEP, cepharanthine; ns, not significant.

Techniques Used: Control

CEP induces ΔΨm loss in triple-negative breast cancer cells. (A) MDA-MB-231 (10 µM; n=3; 24 h) and (B) Hs578T cells (4 µM; n=3; 24 h). Scale bar, 100 µM. CEP, cepharanthine.

Figure Legend Snippet: CEP induces ΔΨm loss in triple-negative breast cancer cells. (A) MDA-MB-231 (10 µM; n=3; 24 h) and (B) Hs578T cells (4 µM; n=3; 24 h). Scale bar, 100 µM. CEP, cepharanthine.

Techniques Used:

CEP upregulates NOXA and downregulates Bcl-2 expression in triple-negative breast cancer cells. CEP upregulated NOXA and downregulated Bcl-2 expression in (A) MDA-MB-231 cells (n=3; 24 h) and (B) Hs578T cells (n=3; 24 h). *P<0.05, **P<0.01 and ***P<0.001 vs. control. CEP, cepharanthine; NOXA, phorbol-12-myristate-13-acetate-induced protein 1; ns, not significant.

Figure Legend Snippet: CEP upregulates NOXA and downregulates Bcl-2 expression in triple-negative breast cancer cells. CEP upregulated NOXA and downregulated Bcl-2 expression in (A) MDA-MB-231 cells (n=3; 24 h) and (B) Hs578T cells (n=3; 24 h). *P<0.05, **P<0.01 and ***P<0.001 vs. control. CEP, cepharanthine; NOXA, phorbol-12-myristate-13-acetate-induced protein 1; ns, not significant.

Techniques Used: Expressing, Control

Proteomic profiling of MDA-MB-231 cells following CEP treatment. (A) The 20 most significantly downregulated Gene Ontology cellular components with CEP treatment. (B) Significantly downregulated Kyoto Encyclopedia of Genes and Genomes pathways with CEP treatment. CEP, cepharanthine.

Figure Legend Snippet: Proteomic profiling of MDA-MB-231 cells following CEP treatment. (A) The 20 most significantly downregulated Gene Ontology cellular components with CEP treatment. (B) Significantly downregulated Kyoto Encyclopedia of Genes and Genomes pathways with CEP treatment. CEP, cepharanthine.

Techniques Used:

CEP treatment activates TFEB in triple-negative breast cancer cells. (A) CEP triggers TFEB nuclear translocation in MDA-MB-231 cells (10 µM; 24 h). (B) CEP triggers TFEB nuclear translocation in Hs578T cells (4 µM; 24 h). Scale bar, 25 µm; n=5. **P<0.01 vs. control. TFEB, transcription factor EB; CEP, cepharanthine.

Figure Legend Snippet: CEP treatment activates TFEB in triple-negative breast cancer cells. (A) CEP triggers TFEB nuclear translocation in MDA-MB-231 cells (10 µM; 24 h). (B) CEP triggers TFEB nuclear translocation in Hs578T cells (4 µM; 24 h). Scale bar, 25 µm; n=5. **P<0.01 vs. control. TFEB, transcription factor EB; CEP, cepharanthine.

Techniques Used: Translocation Assay, Control

CEP does not induce LMP, increase lysosomal pH or destabilize lysosomal membrane-bound enzymes in triple-negative breast cancer cells. (A) CEP does not induce LMP, as evidenced by a dispersion of dextran, in MDA-MB-231 (10 µM; 24 h) and Hs578T cells (4 µM; 24 h). Scale bar, 25 µm. (B) CEP does not elevate lysosomal pH in the MDA-MB-231 (10 µM; 24 h) and Hs578T cell lines (4 µM; 24 h). Scale bar, 25 µm. (C) CEP does not induce lysosomal membrane-bound enzymes degradation in the MDA-MB-231 (10 µM; n=3; 24 h) and Hs578T cell lines (4 µM; n=3; 24 h). CEP, cepharanthine; ASAH1, acid ceramidase; SMPD1, sphingomyelin phosphodiesterase; ns, not significant.

Figure Legend Snippet: CEP does not induce LMP, increase lysosomal pH or destabilize lysosomal membrane-bound enzymes in triple-negative breast cancer cells. (A) CEP does not induce LMP, as evidenced by a dispersion of dextran, in MDA-MB-231 (10 µM; 24 h) and Hs578T cells (4 µM; 24 h). Scale bar, 25 µm. (B) CEP does not elevate lysosomal pH in the MDA-MB-231 (10 µM; 24 h) and Hs578T cell lines (4 µM; 24 h). Scale bar, 25 µm. (C) CEP does not induce lysosomal membrane-bound enzymes degradation in the MDA-MB-231 (10 µM; n=3; 24 h) and Hs578T cell lines (4 µM; n=3; 24 h). CEP, cepharanthine; ASAH1, acid ceramidase; SMPD1, sphingomyelin phosphodiesterase; ns, not significant.

Techniques Used: Membrane, Dispersion

CEP binds to and inhibits lysosomal enzymes. (A) Structurally altered peptides in the MDA-MB-231 cell line upon CEP treatment (10 µM, 1 h; FC >1.5 or <0.667, false discovery rate <1, P<0.01; n=3). (B) CEP treatment suppresses the maturation of CTSB and CTSD (24 h). *P<0.05, **P<0.01 and ***P<0.001 vs. control. CEP, cepharanthine; FC, fold change; CTSD, cathepsin D; CTSB, cathepsin B; pro-CTSB pro-cathepsin B; pro-CTSD, pro-cathepsin D; i-CTSB, inactive cathepsin B; m-CTSB, mature cathepsin B; m-CTSD, mature cathepsin D.

Figure Legend Snippet: CEP binds to and inhibits lysosomal enzymes. (A) Structurally altered peptides in the MDA-MB-231 cell line upon CEP treatment (10 µM, 1 h; FC >1.5 or <0.667, false discovery rate <1, P<0.01; n=3). (B) CEP treatment suppresses the maturation of CTSB and CTSD (24 h). *P<0.05, **P<0.01 and ***P<0.001 vs. control. CEP, cepharanthine; FC, fold change; CTSD, cathepsin D; CTSB, cathepsin B; pro-CTSB pro-cathepsin B; pro-CTSD, pro-cathepsin D; i-CTSB, inactive cathepsin B; m-CTSB, mature cathepsin B; m-CTSD, mature cathepsin D.

Techniques Used: Control

Image Search Results

Journal: Molecular Medicine Reports

Article Title: Cepharanthine inhibits lysosomes and induces apoptosis in triple-negative breast cancer cells

doi: 10.3892/mmr.2026.13899

Figure Lengend Snippet: CEP exerts cytotoxicity in TNBC cells. (A) Chemical structure of CEP. (B) CEP inhibited TNBC cell viability. The effect of CEP treatment on TNBC cell viability after 24, 48 and 72 h. (C) CEP inhibited clonogenicity of MDA-MB-231 and Hs578T cells. n=3; *P < 0.05, **P < 0.01 and ***P < 0.001 vs. control. CEP, cepharanthine; TNBC, triple-negative breast cancer.

Article Snippet: The TNBC cell lines MDA-MB-231 (cat. no. CL-0150; Procell Life Science & Technology Co., Ltd.) and Hs578T (cat. no. CL-0114; Procell Life Science & Technology Co., Ltd.) were cultured in high-glucose DMEM medium (cat. no. C11965500BT; Gibco; Thermo Fisher Scientific, Inc.), supplemented with 10% fetal bovine serum (cat. no. 164210; Procell Life Science & Technology Co., Ltd.) and 1% penicillin/streptomycin (cat. no. 15140122; Gibco; Thermo Fisher Scientific, Inc.).

Techniques: Control

Journal: Molecular Medicine Reports

Article Title: Cepharanthine inhibits lysosomes and induces apoptosis in triple-negative breast cancer cells

doi: 10.3892/mmr.2026.13899

Figure Lengend Snippet: CEP induces apoptosis in triple-negative breast cancer cells. Flow cytometric quantification of apoptosis induced by CEP in (A) MDA-MB-231 and (B) Hs578T cells (n=3; 48 h). **P<0.01 and ***P < 0.001 vs. control. CEP, cepharanthine; ns, not significant.

Techniques: Control

Journal: Molecular Medicine Reports

Article Title: Cepharanthine inhibits lysosomes and induces apoptosis in triple-negative breast cancer cells

doi: 10.3892/mmr.2026.13899

Figure Lengend Snippet: CEP induces ΔΨm loss in triple-negative breast cancer cells. (A) MDA-MB-231 (10 µM; n=3; 24 h) and (B) Hs578T cells (4 µM; n=3; 24 h). Scale bar, 100 µM. CEP, cepharanthine.

Techniques:

Journal: Molecular Medicine Reports

Article Title: Cepharanthine inhibits lysosomes and induces apoptosis in triple-negative breast cancer cells

doi: 10.3892/mmr.2026.13899

Figure Lengend Snippet: CEP upregulates NOXA and downregulates Bcl-2 expression in triple-negative breast cancer cells. CEP upregulated NOXA and downregulated Bcl-2 expression in (A) MDA-MB-231 cells (n=3; 24 h) and (B) Hs578T cells (n=3; 24 h). *P<0.05, **P<0.01 and ***P<0.001 vs. control. CEP, cepharanthine; NOXA, phorbol-12-myristate-13-acetate-induced protein 1; ns, not significant.

Techniques: Expressing, Control

Journal: Molecular Medicine Reports

Article Title: Cepharanthine inhibits lysosomes and induces apoptosis in triple-negative breast cancer cells

doi: 10.3892/mmr.2026.13899

Figure Lengend Snippet: Proteomic profiling of MDA-MB-231 cells following CEP treatment. (A) The 20 most significantly downregulated Gene Ontology cellular components with CEP treatment. (B) Significantly downregulated Kyoto Encyclopedia of Genes and Genomes pathways with CEP treatment. CEP, cepharanthine.

Techniques:

Journal: Molecular Medicine Reports

Article Title: Cepharanthine inhibits lysosomes and induces apoptosis in triple-negative breast cancer cells

doi: 10.3892/mmr.2026.13899

Figure Lengend Snippet: CEP treatment activates TFEB in triple-negative breast cancer cells. (A) CEP triggers TFEB nuclear translocation in MDA-MB-231 cells (10 µM; 24 h). (B) CEP triggers TFEB nuclear translocation in Hs578T cells (4 µM; 24 h). Scale bar, 25 µm; n=5. **P<0.01 vs. control. TFEB, transcription factor EB; CEP, cepharanthine.

Techniques: Translocation Assay, Control

Journal: Molecular Medicine Reports

Article Title: Cepharanthine inhibits lysosomes and induces apoptosis in triple-negative breast cancer cells

doi: 10.3892/mmr.2026.13899

Figure Lengend Snippet: CEP does not induce LMP, increase lysosomal pH or destabilize lysosomal membrane-bound enzymes in triple-negative breast cancer cells. (A) CEP does not induce LMP, as evidenced by a dispersion of dextran, in MDA-MB-231 (10 µM; 24 h) and Hs578T cells (4 µM; 24 h). Scale bar, 25 µm. (B) CEP does not elevate lysosomal pH in the MDA-MB-231 (10 µM; 24 h) and Hs578T cell lines (4 µM; 24 h). Scale bar, 25 µm. (C) CEP does not induce lysosomal membrane-bound enzymes degradation in the MDA-MB-231 (10 µM; n=3; 24 h) and Hs578T cell lines (4 µM; n=3; 24 h). CEP, cepharanthine; ASAH1, acid ceramidase; SMPD1, sphingomyelin phosphodiesterase; ns, not significant.

Techniques: Membrane, Dispersion

Journal: Molecular Medicine Reports

Article Title: Cepharanthine inhibits lysosomes and induces apoptosis in triple-negative breast cancer cells

doi: 10.3892/mmr.2026.13899

Figure Lengend Snippet: CEP binds to and inhibits lysosomal enzymes. (A) Structurally altered peptides in the MDA-MB-231 cell line upon CEP treatment (10 µM, 1 h; FC >1.5 or <0.667, false discovery rate <1, P<0.01; n=3). (B) CEP treatment suppresses the maturation of CTSB and CTSD (24 h). *P<0.05, **P<0.01 and ***P<0.001 vs. control. CEP, cepharanthine; FC, fold change; CTSD, cathepsin D; CTSB, cathepsin B; pro-CTSB pro-cathepsin B; pro-CTSD, pro-cathepsin D; i-CTSB, inactive cathepsin B; m-CTSB, mature cathepsin B; m-CTSD, mature cathepsin D.

Techniques: Control

Brain pericyte secretions mediate the inhibition of TNBC cell adhesion to the BBB. (A) Experimental workflow for adhesion assay. All BBB experiments were performed using ECGMV2 medium with supplements for all conditions from day −6 to the end of the experiment. The astrocyte medium was renewed 24 h before the adhesion experiment with the same ECGMV2 medium. Endothelial cells (ECs) and brain pericytes (hBPs) were co‐cultured for 5 days, and inserts containing brain‐like endothelial cells (hBLECs) were then either maintained with hBPs or transferred to wells without hBPs. After 24 hours, and prior to MDA‐MB‐231 cells seeding, inserts were subjected to the following conditions: maintained without hBPs (hBLEC 24h); transferred to hBPs previously cultured alone for 24 hours (hBLEC 24h then hBP); transferred to wells without hBPs but containing either culture medium (hBLEC) or CM from co‐culture (hBLEC + CM coc ); transferred to wells with astrocytes (hBLEC + A) or maintained in co‐culture with hBPs (hBLEC + hBP). (B–G), Quantification (B, D, F) of MDA‐MB‐231 cell adhesion to hBLECs after 3 h of incubation and representative images (C, E, G) of adhered MDA‐MB‐231 cells (green) under the different conditions. Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using one‐way ANOVA followed by Tukey's test (B), Welch's ANOVA followed by Dunnett's T3 test (D) and Kruskal–Wallis test followed by Dunn's test (F). CM coc = conditioned medium from 24 h hBLECs and hBPs coculture, A = astrocytes, hBP mono = 24 h hBPs monoculture. Scale bar = 750 µm. BBB, blood–brain barrier; ECGMV2, EC Growth Medium MV 2; ECs, endothelial cells; hBLECs, human brain‐like endothelial cells; ns, non‐significant; hBPs, human brain pericytes; TNBC, triple‐negative breast cancer. **** p ≤ 0.0001; * p ≤ 0.05.

Journal: Journal of Cell Communication and Signaling

Article Title: Human brain pericytes protect the blood–brain barrier from triple‐negative breast cancer cells while promoting tumor aggressiveness

doi: 10.1002/ccs3.70070

Figure Lengend Snippet: Brain pericyte secretions mediate the inhibition of TNBC cell adhesion to the BBB. (A) Experimental workflow for adhesion assay. All BBB experiments were performed using ECGMV2 medium with supplements for all conditions from day −6 to the end of the experiment. The astrocyte medium was renewed 24 h before the adhesion experiment with the same ECGMV2 medium. Endothelial cells (ECs) and brain pericytes (hBPs) were co‐cultured for 5 days, and inserts containing brain‐like endothelial cells (hBLECs) were then either maintained with hBPs or transferred to wells without hBPs. After 24 hours, and prior to MDA‐MB‐231 cells seeding, inserts were subjected to the following conditions: maintained without hBPs (hBLEC 24h); transferred to hBPs previously cultured alone for 24 hours (hBLEC 24h then hBP); transferred to wells without hBPs but containing either culture medium (hBLEC) or CM from co‐culture (hBLEC + CM coc ); transferred to wells with astrocytes (hBLEC + A) or maintained in co‐culture with hBPs (hBLEC + hBP). (B–G), Quantification (B, D, F) of MDA‐MB‐231 cell adhesion to hBLECs after 3 h of incubation and representative images (C, E, G) of adhered MDA‐MB‐231 cells (green) under the different conditions. Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using one‐way ANOVA followed by Tukey's test (B), Welch's ANOVA followed by Dunnett's T3 test (D) and Kruskal–Wallis test followed by Dunn's test (F). CM coc = conditioned medium from 24 h hBLECs and hBPs coculture, A = astrocytes, hBP mono = 24 h hBPs monoculture. Scale bar = 750 µm. BBB, blood–brain barrier; ECGMV2, EC Growth Medium MV 2; ECs, endothelial cells; hBLECs, human brain‐like endothelial cells; ns, non‐significant; hBPs, human brain pericytes; TNBC, triple‐negative breast cancer. **** p ≤ 0.0001; * p ≤ 0.05.

Article Snippet: The human TNBC cell line MDA‐MB‐231 (female) was obtained from the American type culture collection (ATCC, HTB‐26, RRID:CVCL_0062, obtained in 2023).

Techniques: Inhibition, Cell Adhesion Assay, Cell Culture, Co-Culture Assay, Incubation

Brain pericytes maintain BBB integrity in the presence of TNBC cells. (A–E) Endothelial permeability (Pe) to Lucifer Yellow assessed after 3 h (A) or 16 h (C) of incubation with MDA‐MB‐231 cells, in the presence or absence of brain pericytes (hBPs). Permeability was also measured in the absence of cancer cells as a control. Permeability values (expressed in × 10 −3 cm/min ± SD) are summarized in a table (E). Representative images of endothelial Claudin‐5 (magenta) immunostaining in the absence or presence of hBPs after 3 h (B) or 16 h (D) of incubation with MDA‐MB‐231 cells (green). Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using one‐way ANOVA followed by Tukey's test (A) and Welch's ANOVA followed by Dunnett's T3 test (B). MDA = MDA‐MB‐231 cells. Scale bars = 300 μm (10X) and 100 μm (40X). BBB, blood–brain barrier; hBPs, human brain pericytes; ns, non‐significant; TNBC, triple‐negative breast cancer. *** p ≤ 0.001; ** p ≤ 0.01; * p ≤ 0.05.

Journal: Journal of Cell Communication and Signaling

Article Title: Human brain pericytes protect the blood–brain barrier from triple‐negative breast cancer cells while promoting tumor aggressiveness

doi: 10.1002/ccs3.70070

Figure Lengend Snippet: Brain pericytes maintain BBB integrity in the presence of TNBC cells. (A–E) Endothelial permeability (Pe) to Lucifer Yellow assessed after 3 h (A) or 16 h (C) of incubation with MDA‐MB‐231 cells, in the presence or absence of brain pericytes (hBPs). Permeability was also measured in the absence of cancer cells as a control. Permeability values (expressed in × 10 −3 cm/min ± SD) are summarized in a table (E). Representative images of endothelial Claudin‐5 (magenta) immunostaining in the absence or presence of hBPs after 3 h (B) or 16 h (D) of incubation with MDA‐MB‐231 cells (green). Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using one‐way ANOVA followed by Tukey's test (A) and Welch's ANOVA followed by Dunnett's T3 test (B). MDA = MDA‐MB‐231 cells. Scale bars = 300 μm (10X) and 100 μm (40X). BBB, blood–brain barrier; hBPs, human brain pericytes; ns, non‐significant; TNBC, triple‐negative breast cancer. *** p ≤ 0.001; ** p ≤ 0.01; * p ≤ 0.05.

Article Snippet: The human TNBC cell line MDA‐MB‐231 (female) was obtained from the American type culture collection (ATCC, HTB‐26, RRID:CVCL_0062, obtained in 2023).

Techniques: Permeability, Incubation, Control, Immunostaining

Brain pericytes limit TNBC cell adhesion to the BBB under hypoxic conditions. (A) Experimental workflow for adhesion assay in hypoxic conditions. All BBB experiments were performed using ECGMV2 medium with supplements for all conditions from day −6 to the end of the experiment. After 5 days of co‐culture with brain pericytes (hBPs), inserts containing brain‐like endothelial cells (hBLECs) were exposed to hypoxia for 24 h in the presence or absence of hBPs. Parallel conditions maintained in normoxia served as controls. (B–E) Quantification (B, D) of MDA‐MB‐231 cell adhesion to hBLECs after 3 h of incubation and representative images (C, E) of adhered MDA‐MB‐231 cells (green) under the different conditions. Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using Welch's ANOVA followed by Dunnett's T3 test (B) and Kruskal‐Wallis test followed by Dunn's test (D). hBP‐CM mono = conditioned medium from 24 h hBPs monoculture. Scale bar = 750 μm. BBB, blood–brain barrier; ECGMV2, EC Growth Medium MV 2; hBLECs, human brain‐like endothelial cells; hBPs, human brain pericytes; ns, non‐significant; TNBC, triple‐negative breast cancer. *** p ≤ 0.001; ** p ≤ 0.01; * p ≤ 0.05.

Journal: Journal of Cell Communication and Signaling

Article Title: Human brain pericytes protect the blood–brain barrier from triple‐negative breast cancer cells while promoting tumor aggressiveness

doi: 10.1002/ccs3.70070

Figure Lengend Snippet: Brain pericytes limit TNBC cell adhesion to the BBB under hypoxic conditions. (A) Experimental workflow for adhesion assay in hypoxic conditions. All BBB experiments were performed using ECGMV2 medium with supplements for all conditions from day −6 to the end of the experiment. After 5 days of co‐culture with brain pericytes (hBPs), inserts containing brain‐like endothelial cells (hBLECs) were exposed to hypoxia for 24 h in the presence or absence of hBPs. Parallel conditions maintained in normoxia served as controls. (B–E) Quantification (B, D) of MDA‐MB‐231 cell adhesion to hBLECs after 3 h of incubation and representative images (C, E) of adhered MDA‐MB‐231 cells (green) under the different conditions. Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using Welch's ANOVA followed by Dunnett's T3 test (B) and Kruskal‐Wallis test followed by Dunn's test (D). hBP‐CM mono = conditioned medium from 24 h hBPs monoculture. Scale bar = 750 μm. BBB, blood–brain barrier; ECGMV2, EC Growth Medium MV 2; hBLECs, human brain‐like endothelial cells; hBPs, human brain pericytes; ns, non‐significant; TNBC, triple‐negative breast cancer. *** p ≤ 0.001; ** p ≤ 0.01; * p ≤ 0.05.

Article Snippet: The human TNBC cell line MDA‐MB‐231 (female) was obtained from the American type culture collection (ATCC, HTB‐26, RRID:CVCL_0062, obtained in 2023).

Techniques: Cell Adhesion Assay, Co-Culture Assay, Incubation

Brain pericytes maintain BBB integrity in the presence of TNBC cells under hypoxic conditions and supplement deprivation. (A) After 5 days of co‐culture with brain pericytes (hBPs) in ECGMV2 medium with supplements, inserts containing brain‐like endothelial cells (hBLECs) co‐cultured with hBPs were exposed to hypoxia for 16 h following medium replacement with ECGMV2 basal medium (without supplements). Then, endothelial permeability (Pe) to Lucifer Yellow was assessed after 3 h of incubation with MDA‐MB‐231 cells, in the presence or absence of hBPs, under normoxic and hypoxic conditions. (B) Permeability values (expressed in x10 −3 cm/min ± SD) are summarized in a table. (C) Representative images of endothelial Claudin‐5 (magenta) immunostaining in the absence or presence of hBPs after 3 h of incubation with MDA‐MB‐231 cells (green) under hypoxic conditions in basal medium. Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using Welch's ANOVA followed by Dunnett's T3 test. MDA = MDA‐MB‐231 cells. Scale bars = 300 μm (10X) and 100 μm (40X). BBB, blood–brain barrier; ECGMV2, EC Growth Medium MV 2; hBLECs, human brain‐like endothelial cells; hBPs, human brain pericytes; ns, non‐significant; TNBC, triple‐negative breast cancer. *** p ≤ 0.001; ** p ≤ 0.01; * p ≤ 0.05.

Journal: Journal of Cell Communication and Signaling

Article Title: Human brain pericytes protect the blood–brain barrier from triple‐negative breast cancer cells while promoting tumor aggressiveness

doi: 10.1002/ccs3.70070

Figure Lengend Snippet: Brain pericytes maintain BBB integrity in the presence of TNBC cells under hypoxic conditions and supplement deprivation. (A) After 5 days of co‐culture with brain pericytes (hBPs) in ECGMV2 medium with supplements, inserts containing brain‐like endothelial cells (hBLECs) co‐cultured with hBPs were exposed to hypoxia for 16 h following medium replacement with ECGMV2 basal medium (without supplements). Then, endothelial permeability (Pe) to Lucifer Yellow was assessed after 3 h of incubation with MDA‐MB‐231 cells, in the presence or absence of hBPs, under normoxic and hypoxic conditions. (B) Permeability values (expressed in x10 −3 cm/min ± SD) are summarized in a table. (C) Representative images of endothelial Claudin‐5 (magenta) immunostaining in the absence or presence of hBPs after 3 h of incubation with MDA‐MB‐231 cells (green) under hypoxic conditions in basal medium. Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using Welch's ANOVA followed by Dunnett's T3 test. MDA = MDA‐MB‐231 cells. Scale bars = 300 μm (10X) and 100 μm (40X). BBB, blood–brain barrier; ECGMV2, EC Growth Medium MV 2; hBLECs, human brain‐like endothelial cells; hBPs, human brain pericytes; ns, non‐significant; TNBC, triple‐negative breast cancer. *** p ≤ 0.001; ** p ≤ 0.01; * p ≤ 0.05.

Article Snippet: The human TNBC cell line MDA‐MB‐231 (female) was obtained from the American type culture collection (ATCC, HTB‐26, RRID:CVCL_0062, obtained in 2023).

Techniques: Co-Culture Assay, Cell Culture, Permeability, Incubation, Immunostaining

Brain pericytes enhance migratory and invasion properties of TNBC cells. (A) Quantification of MDA‐MB‐231 cells that migrated to the lower side of insert filters in the absence (∅) or presence of brain pericytes (+hBPs), and representative images of migrated cells (nuclei stained in blue) associated. (B) Quantification of MDA‐MB‐231 cells that invaded the lower side of insert filters pre‐coated with Matrigel ® in the presence (+hBP) or absence (∅) of hBPs. (C) Representative images of MDA‐MB‐231 cells (green) after 48 h of monoculture or co‐culture with hBPs; cell morphology is visualized by F‐actin staining (phalloidin, orange). (D) Heatmap visualization of F‐actin intensity. (E) Quantification of cortical F‐actin fluorescence in MDA‐MB‐231 cells. (F) MDA‐MB‐231 cell elongation factor, defined as the ratio of cell length to width, following 48 h of monoculture (MDA) and co‐culture with hBPs (MDA + hBP), or following 1‐hour treatment with DMEM 0.1% (CTL medium) and hBP‐CM. Data are obtained from three independent experiments, with three technical replicates (A, B) or at least 30 cells analyzed (E, F) per condition. Statistical analyses were performed using a Mann–Whitney test (A, E, F) and an unpaired t ‐test with Welch's correction (B). MDA = MDA‐MB‐231 cells. Scale bars = 750 μm (A) and 100 μm (C, D). DMEM, Dulbecco'’s Modified Eagle Medium; hBP‐CM, hBP‐conditioned medium; hBPs, human brain pericytes; TNBC, triple‐negative breast cancer. **** p ≤ 0.0001; * p ≤ 0.05.

Journal: Journal of Cell Communication and Signaling

Article Title: Human brain pericytes protect the blood–brain barrier from triple‐negative breast cancer cells while promoting tumor aggressiveness

doi: 10.1002/ccs3.70070

Figure Lengend Snippet: Brain pericytes enhance migratory and invasion properties of TNBC cells. (A) Quantification of MDA‐MB‐231 cells that migrated to the lower side of insert filters in the absence (∅) or presence of brain pericytes (+hBPs), and representative images of migrated cells (nuclei stained in blue) associated. (B) Quantification of MDA‐MB‐231 cells that invaded the lower side of insert filters pre‐coated with Matrigel ® in the presence (+hBP) or absence (∅) of hBPs. (C) Representative images of MDA‐MB‐231 cells (green) after 48 h of monoculture or co‐culture with hBPs; cell morphology is visualized by F‐actin staining (phalloidin, orange). (D) Heatmap visualization of F‐actin intensity. (E) Quantification of cortical F‐actin fluorescence in MDA‐MB‐231 cells. (F) MDA‐MB‐231 cell elongation factor, defined as the ratio of cell length to width, following 48 h of monoculture (MDA) and co‐culture with hBPs (MDA + hBP), or following 1‐hour treatment with DMEM 0.1% (CTL medium) and hBP‐CM. Data are obtained from three independent experiments, with three technical replicates (A, B) or at least 30 cells analyzed (E, F) per condition. Statistical analyses were performed using a Mann–Whitney test (A, E, F) and an unpaired t ‐test with Welch's correction (B). MDA = MDA‐MB‐231 cells. Scale bars = 750 μm (A) and 100 μm (C, D). DMEM, Dulbecco'’s Modified Eagle Medium; hBP‐CM, hBP‐conditioned medium; hBPs, human brain pericytes; TNBC, triple‐negative breast cancer. **** p ≤ 0.0001; * p ≤ 0.05.

Article Snippet: The human TNBC cell line MDA‐MB‐231 (female) was obtained from the American type culture collection (ATCC, HTB‐26, RRID:CVCL_0062, obtained in 2023).

Techniques: Staining, Co-Culture Assay, Fluorescence, MANN-WHITNEY, Modification

Brain pericyte secretions enhance TNBC clonogenic capacity. (A) Representative images of MDA‐MB‐231 colony formation following exposure to conditioned medium from brain pericytes (hBP‐CM), control medium (DMEM 0.1%, medium used for CM generation), or DMEM 10%. (B) Quantification of colony numbers formed by MDA‐MB‐231 under previously indicated conditions. Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using a Mann–Whitney test. MDA = MDA‐MB‐231 cells. Scale bar = 600 μm. DMEM, Dulbecco'’s Modified Eagle Medium; hBP‐CM, hBP‐conditioned medium; TNBC, triple‐negative breast cancer.

Journal: Journal of Cell Communication and Signaling

Article Title: Human brain pericytes protect the blood–brain barrier from triple‐negative breast cancer cells while promoting tumor aggressiveness

doi: 10.1002/ccs3.70070

Figure Lengend Snippet: Brain pericyte secretions enhance TNBC clonogenic capacity. (A) Representative images of MDA‐MB‐231 colony formation following exposure to conditioned medium from brain pericytes (hBP‐CM), control medium (DMEM 0.1%, medium used for CM generation), or DMEM 10%. (B) Quantification of colony numbers formed by MDA‐MB‐231 under previously indicated conditions. Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using a Mann–Whitney test. MDA = MDA‐MB‐231 cells. Scale bar = 600 μm. DMEM, Dulbecco'’s Modified Eagle Medium; hBP‐CM, hBP‐conditioned medium; TNBC, triple‐negative breast cancer.

Article Snippet: The human TNBC cell line MDA‐MB‐231 (female) was obtained from the American type culture collection (ATCC, HTB‐26, RRID:CVCL_0062, obtained in 2023).

Techniques: Control, MANN-WHITNEY, Modification

ALDH activity in triple-negative breast cancer MDA-MB-231 and invasive ductal carcinoma-derived KAIMRC1 cells measurements using a colorimetric assay. KAIMRC1 stem-like cells showed higher ALDH activity when compared with that of MDA-MB-231 cells. Data are presented as the mean ± SD from three independent experiments. Statistical significance relative to MDA-MB-231 cells is indicated as *P<0.05. ALDH, aldehyde dehydrogenase.

Journal: Oncology Letters

Article Title: Methylglyoxal-derived glycated albumin enhances the stemness potential of invasive ductal carcinoma-derived breast cancer stem-like cell line KAIMRC1

doi: 10.3892/ol.2026.15541

Figure Lengend Snippet: ALDH activity in triple-negative breast cancer MDA-MB-231 and invasive ductal carcinoma-derived KAIMRC1 cells measurements using a colorimetric assay. KAIMRC1 stem-like cells showed higher ALDH activity when compared with that of MDA-MB-231 cells. Data are presented as the mean ± SD from three independent experiments. Statistical significance relative to MDA-MB-231 cells is indicated as *P<0.05. ALDH, aldehyde dehydrogenase.

Article Snippet: The TNBC cell line MDA-MB-231 (cat. no. HTB-26, American Type Culture Collection) was maintained in complete DMEM supplemented with the aforementioned components.

Techniques: Activity Assay, Derivative Assay, Colorimetric Assay

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